Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

Zhang, Chong-Yang; Yuan, Wei-Gang; He, Pei; Lei, Jia-Hui; Wang, Chun-Xu

doi:10.3748/wjg.v22.i48.10512

Cited by 596Liver physiology and pathologyLiver Disease Diagnosis and TreatmentLiver Disease and Transplantation

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

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Zhang, Chong-Yang, Yuan, Wei-Gang, He, Pei, Lei, Jia-Hui, Wang, Chun-Xu·2016·World Journal of Gastroenterology

DOI 10.3748/wjg.v22.i48.10512PMC PMC5192262

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Abstract

Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation.Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown.Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic.Importantly, hepatic stellate cells (HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis.These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage.Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets.This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis.

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Hepatic stellate cells, characterized by DES and VIM expressions, are central to liver fibrosis and extracellular matrix remodeling.
“Hepatic stellate cells, characterized by DES and VIM expressions, are central to liver fibrosis and extracellular matrix remodeling34,36.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
The Introduction says activated hepatic stellate cells drive fibrosis and secrete proteins involved in extracellular matrix remodeling. The Etiology and Pathological Characteristics section identifies desmin (DES) as upregulated when stellate cells activate, but our copy does not identify VIM expression as a characteristic; it also confines the DES finding to activated cells. Page numbers were not available in the indexed passages. (LLM, conf=0.88)
Experimental — accuracy not yet measured
The mesenchymal shift by Day 45 suggests greater cellular complexity at later stages, potentially facilitating iHLO use in modeling liver pathologies such as fibrosis, cirrhosis, and liver remodeling, as indicated by increased expression of hepatic stellate cell markers DES and VIM.
“Interestingly, the mesenchymal shift by Day 45 suggests greater cellular complexity at later stages, potentially facilitating iHLO use in modeling liver pathologies such as fibrosis, cirrhosis, and liver remodeling, as indicated by increased expression of hepatic stellate cell markers such as DES and VIM33,34.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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The expansion of the mesenchymal-like population at Day 45 suggests that these organoids could serve as an advanced model for studying fibrogenesis and testing anti-fibrotic therapies.
“The expansion of mesenchymal-like population at Day 45 suggests that these organoids could serve as an advanced model for studying fibrogenesis and testing anti-fibrotic therapies34.”
From Temporal proteomic profiling of iPSC-derived human liver organoids reveals optimal maturation for drug metabolism and toxicology (2026) · cites this paper as [34]
The review’s “Animal models of liver fibrogenesis” section discusses animal models, and its therapeutic-target sections discuss hepatic stellate cells and antifibrotic approaches. Searches for organoids, a Day 45 mesenchymal-like population, and organoid-based therapy testing found no passage addressing the claim about these organoids. (LLM, conf=0.76)
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Wound healing, fibroblast heterogeneity, and fibrosis
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Adoptive Transfer of Bone Marrow-Derived Monocytes Ameliorates Schistosoma mansoni -Induced Liver Fibrosis in Mice
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MyD88 in hepatic stellate cells enhances liver fibrosis via promoting macrophage M1 polarization
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Mesenchymal stem cell-originated exosomal circDIDO1 suppresses hepatic stellate cell activation by miR-141-3p/PTEN/AKT pathway in human liver fibrosis
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Macrophage in liver Fibrosis: Identities and mechanisms
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T lymphocytes as critical mediators in tissue regeneration, fibrosis, and the foreign body response
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Esculin inhibits hepatic stellate cell activation and CCl4-induced liver fibrosis by activating the Nrf2/GPX4 signaling pathway.
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Pyruvate Kinase M2 Tetramerization Protects against Hepatic Stellate Cell Activation and Liver Fibrosis
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Fibroblast activation protein activated antifibrotic peptide delivery attenuates fibrosis in mouse models of liver fibrosis
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Umbelliferone Ameliorates CCl4-Induced Liver Fibrosis in Rats by Upregulating PPARγ and Attenuating Oxidative Stress, Inflammation, and TGF-β1/Smad3 Signaling
Mahmoud, A. M., Hozayen, W. G., Hasan, I. H., Shaban, E., & Bin-Jumah, M. N. (2019) · Inflammation · doi:10.1007/s10753-019-00973-8 · Cited by 78 · see citing works
Programmed cell death in hepatic fibrosis: current and perspectives
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Hydrogen Sulfide as a Novel Regulatory Factor in Liver Health and Disease
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Novel Insights on Notch signaling pathways in liver fibrosis
Ni, M.-M., Wang, Y.-R., Wu, W., Xia, C.-C., Zhang, Y.-H., Xu, J., Xu, T., & Li, J. (2018) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2018.02.051 · Cited by 73 · see citing works
Peroxisome proliferator-activated receptors in the pathogenesis and therapies of liver fibrosis
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The Role of S1P and the Related Signaling Pathway in the Development of Tissue Fibrosis
Wang, E., He, X., & Zeng, M. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2018.01504 · Cited by 69 · see citing works
PPARγ/NF‐κB and TGF‐β1/Smad pathway are involved in the anti‐fibrotic effects of levo‐tetrahydropalmatine on liver fibrosis
Yu, Q., Cheng, P., Wu, J., & Guo, C. (2021) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.16267 · Cited by 69 · see citing works
Oxidative Stress and Redox Signaling in the Pathophysiology of Liver Diseases
Mooli, R. G. R., Mukhi, D., & Ramakrishnan, S. K. (2022) · Comprehensive physiology · doi:10.1002/cphy.c200021 · Cited by 128 · see citing works
Eosinophils and Macrophages within the Th2-Induced Granuloma: Balancing Killing and Healing in a Tight Space
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Matrix metalloproteinase-1 decorated polymersomes, a surface-active extracellular matrix therapeutic, potentiates collagen degradation and attenuates early liver fibrosis
Geervliet, E., Moreno, S., Baiamonte, L., Booijink, R. S., Boye, S., Wang, P., Voit, B. I., Lederer, A., Appelhans, D., & Bansal, R. (2021) · Journal of Controlled Release · doi:10.1016/j.jconrel.2021.03.016 · Cited by 65 · see citing works
Investigation of the relationship between CTLA4 and the tumor suppressor RASSF1A and the possible mediating role of STAT4 in a cohort of Egyptian patients infected with hepatitis C virus with and without hepatocellular carcinoma
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Nuclear factor erythroid 2-related factor 2-mediated signaling and metabolic associated fatty liver disease
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Foxp3+ Regulatory T Cells Inhibit CCl4-Induced Liver Inflammation and Fibrosis by Regulating Tissue Cellular Immunity
Ikeno, Y., Ohara, D., Takeuchi, Y., Watanabe, H., Kondoh, G., Taura, K., Uemoto, S., & Hirota, K. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.584048 · Cited by 62 · see citing works
Lipids associated with autophagy: mechanisms and therapeutic targets
Jarocki, M., Turek, K., Saczko, J., Tarek, M., & Kulbacka, J. (2024) · Cell Death Discovery · doi:10.1038/s41420-024-02224-8 · Cited by 66 · see citing works
Natural Sulfur-Containing Compounds: An Alternative Therapeutic Strategy against Liver Fibrosis
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Authors: Zhang, C.-Y., Yuan, W.-G., He, P., Lei, J.-H., & Wang, C.-X.
Affiliations: Huazhong University of Science and Technology (CN)
Venue: World Journal of Gastroenterology
Publisher: Baishideng Publishing Group Inc.
Published: 2016
Volume: 22
Issue: 48
Pages: 10512
ISSN: 1007-9327 (ISSN-L)
DOI: 10.3748/wjg.v22.i48.10512
PMC: PMC5192262
OpenAlex: W2565367159
Cited by: 594
References: 112
Citations by year: 2026: 37 · 2025: 70 · 2024: 75 · 2023: 80 · 2022: 84 · 2021: 88 · 2020: 60 · 2019: 59 · 2018: 24 · 2017: 15 · 2012: 1
FWCI: 4.07
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc
Locations: World Journal of Gastroenterology (publishedVersion, cc-by-nc)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
Funders: National Natural Science Foundation of China (81300251)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
Keywords: liver fibrosis, hepatic stellate cells, liver cirrhosis, hepatocellular carcinoma, antifibrotic therapy, fibrogenic factors, collagen synthesis, myofibroblasts, viral hepatitis, schistosomiasis, alcoholic liver disease, cell-cell crosstalk, therapeutic target
MeSH terms: Resveratrol, Ursolic Acid, Acetyl-CoA C-Acetyltransferase, Animals, Fatty Liver, Alcoholic, Humans, Interleukins, Liver Cirrhosis, Macrophages, Schistosomiasis, Stilbenes, Triterpenes, Ursodeoxycholic Acid, Virus Diseases, Signal Transduction, CD4-Positive T-Lymphocytes, Disease Progression, MicroRNAs, Intracellular Signaling Peptides and Proteins, T-Lymphocytes, Regulatory, Hepatic Stellate Cells, Molecular Targeted Therapy, LIM Domain Proteins, Non-alcoholic Fatty Liver Disease

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Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

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